Chlorinated dibenzodioxins (CDDs) and dibenzofurans (CDFs) are found world-wide as environmental pollutants. Previous studies from our laboratory have indicated that metabolism is a prerequisite for elimination and is a detoxification process. Persistence is related to lack of metabolism, but can also be modulated by body composition. These compounds are well absorbed after oral exposure, although 2,3,4,7,8-pentaCDF (4- PeCDF) is not absorbed as well as 2,3,7,8-tetraCDF (TCDF) in either the rat or the monkey. These chemicals, as well as 2,3,7,8- tetrachlorodibenzo-p-dioxin (TCDD) and 1,2,3,7,8-pentaCDF (1- PeCDF) are only poorly absorbed from the skin (equivalent to 20% of an applied dose). In the rat, metabolism follows the following order: TCDF is greater than 1-PeCDF is greater than TCDD is greater than 4-PeCDF. This is inversely relate to the persistence of these compounds with 4-PeCDF having the longest whole-body half-life. 4-PeCDF, which has been shown to be present in the human population, is nearly as toxic as TCDD in the monkey. We have also examine the disposition and toxicity of octachlorodibenzodioxin (OCDD). It is poorly absorbed after oral exposure (less than 10% absorption). However, what is absorbed concentrates and persists in the liver. Repeated exposure results in a linear accumulation of OCDD In the liver and adipose tissue. The whole body half-life is between 3-5 months in the rat, suggesting that steady-state conditions would never be achieved upon continuous, low-level exposure. We exposed rats for as long as 13 weeks, 5 days per week, to OCDD to determine if subchronic exposure would result in any toxic effects. In fact, OCDD caused the same toxic syndrome as that seen upon acute exposure to TCDD: induction of specific hepatic monoxygenases, fatty changes and vacuolization of the liver, a mild, non- regenerative anemia, and increases in bile acids. Thus, OCDD, while only .01-.001X as potent, is TCDD-like in its actions upon repeated exposure.